In our previous study of cerebrotropic melanomas, we found the mechanism accounting for PDCD4 loss or suppression was post-translational, via proteasomal degradation and likely regulated by the crosstalk of PLEKHA5, a mediator of brain metastasis, with the PI3K/AKT and ubiquitin-proteasome pathways [22]. This evidence concerns the gene AKT1 and melanoma.